The I factor of Drosophila melanogaster is the transposable element that controls I-R hybrid dysgenesis. I-Rhybrid dysgenesis is seen when males of strains that have I factors (inducer strains) are crossed with females that lack them (reactive strains). Dysgenesis is manifested only in the female progeny of such a cross (SF females) as reduced hatchability of eggs. The females progeny of the reciprocal cross (RSF females) are fertile. SF sterility correlates with high rates of I factor transposition in the SF germline. The I factor is a LINE-like transposable element, mobility of which is thought to occur by reverse transcription of a full length transcript. This mechanism predicts that the I factor has a promoter internal to the transcription unit. Occurrence of the putative RNA intermediate for I factor transposition correlates with transposition frequency, suggesting that I factor mobility is controlled at the level of transcription or RNA stability. The experiments described in this thesis identify a promoter within the 5' UTR of the I factor that initiates transcription at position + 1. Characterisation of this promoter fused to the CAT reporter gene in transient assays in Drosophila tissue culture cells has identified sequences that modulate expression positively and negatively. Transformation of a reactive strain with analogous I-CAT expression vectors demonstrated that sequences within the first 186 nucleotides of I contribute to elevated levels of expression in ovaries, suppression of promoter activity in males, female somatic tissues, and during development of both males and females. I factor transposition and transcripts are rare in inducer lines. Conversion of transgenic lines to the inducer cytotype reduced CAT expression in the ovaries indicating that the 5' 186bp of I is a target for cytotype regulation. SF and RSF flies produced by matings between transformed and host lines showed that the non-reciprocal maternal effect of I-R dysgenesis also acts on nucleotides 1-186 of I. The implications of these results for transcription mechanisms and transposition regulation are discussed.